Angiogenesis, Inflammation & Therapeutics | Online ISSN  2207-872X
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An insight into chronic kidney diseas (CKD) through an unbalanced angiogenesis

Elham Farsi

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Journal of Angiotherapy 1(1) 036-038 https://doi.org/10.25163/angiotherapy.11000821108100517

Submitted: 11 September 2016  Revised: 17 March 2017  Published: 10 May 2017 

Although findings about the biological role of angiogenesis factors in CKD are relatively limited, therapeutic effects have been reported for angiogenesis factors in experimental diabetic nephropathy models. 

Abstract


Recent research data and supporting animal studies have shown that acute kidney injury (AKI) can eventually lead to chronic kidney disease (CKD). Moreover, the frequency of kidney transplants as result of CKD have been increasing daily. Various renal disorders result in end stage renal failure (ESRF) including glomerulonephritis, hypertensive nephrosclerosis and diabetic nephropathy (Levey and Coresh 2012). Chronic kidney disease involves conditions such as glomerulonephritis, glomerular endothelial cell injuries accompanies mesangial alterations or extracapillary lesions. To retrieve the glomerular endothelial cells in these models, angiogenesis stimulation is required to promote glomerular endothelial repair in association with accelerated resolution of nephritic alterations. The level of angiogenic signal should be adjusted according to the type and the stage of disease, to avoid an imbalance of pro / antigrowth and promotion of other pathologic condition as result of excessive angiogenesis (Goligorsky 2015; Levey and Coresh 2012) . The development of new blood vessels, termed angiogenesis is responsible for several physiological and pathological events such as tumor growth and metastasis, proliferative retinopathy, rheumatoid arthritis, psoriasis and neointimal formation (Risau 1997). This process is controlled by pro and anti- growth factors and it is directly associated with the development of renal failure. Consequently, balanced ratios of these factors control severe renal conditions (Carmeliet 2003) The deregulated expression of factorsinhibitors ends in pathological conditions, like inflammation. Although findings about the biological role of angiogenesis factors in CKD are relatively limited, therapeutic effects have been reported for angiogenesis factors in experimental diabetic nephropathy models. Angiogenesis inhibitors exhibit therapeutic effects on diabetic nephropathy by anti-angiogenic and anti-inflammatory mechanisms. These effects highlight the importance of a tight regulation of angiogenic factors and inhibitors (Tanaka and Nangaku 2013).

Keywords: Chronic Kidney Disease, Angiogenesis

References


Boor, P. and Floege, J. (2011). Chronic kidney disease growth factors in renal fibrosis. Clinical and Experimental Pharmacology and Physiology 38, 441-450.

Carmeliet, P. 2003. Angiogenesis in health and disease. Nature medicine 9, 653-660.

Chen, J., Hamm, L.L., Kleinpeter, M.A., Husserl, F., Khan, I.E., Chen, C.-S., Liu, Y., Mills, K.T., He, C. and Rifai, N. (2012). Elevated plasma levels of endostatin are associated with chronic kidney disease. American journal of nephrology 35, 335-340.

Futrakul, N. and Futrakul, P. (2011). Vascular homeostasis and angiogenesis determine therapeutic effectiveness in type 2 diabetes. International journal of vascular medicine 2011.

Goligorsky, M.S. (2015). Chapter 15 - Chronic Kidney Disease and Vascular Endothelium. In: P.L. Kimmel and M.E. Rosenberg (Eds), Chronic Renal Disease, Academic Press, San Diego, pp. 170-180.

Khamaisi, M., Schrijvers, B.F., De Vriese, A.S., Raz, I. and Flyvbjerg, A. (2003). The emerging role of VEGF in diabetic kidney disease. Nephrology Dialysis Transplantation 18, 1427-1430.

Levey, A.S. and Coresh, J. (2012). Chronic kidney disease. The Lancet 379, 165-180.

Maeshima, Y. and Makino, H. (2010). Angiogenesis and chronic kidney disease. Fibrogenesis Tissue Repair 3, 1-17.

Mu, W., Long, D.A., Ouyang, X., Agarwal, A., Cruz, P.E., Roncal, C.A., Nakagawa, T., Yu, X., Hauswirth, W.W. and Johnson, R.J. (2009). Angiostatin overexpression is associated with an improvement in chronic kidney injury by an anti-inflammatory mechanism. American Journal of Physiology-Renal Physiology 296, F145-F152.

Noiri, E. and Fujita, T. (2010). Role of vascular endothelial growth factor in kidney disease. Current vascular pharmacology 8, 122-128.

Risau, W. (1997). Mechanisms of angiogenesis. Nature 386, 671-674.
Schrijvers, B.F., Flyvbjerg, A. and De Vriese, A.S. (2004). The role of vascular endothelial growth factor (VEGF) in renal pathophysiology. Kidney Int 65, 2003-2017.

Tanaka, T. and Nangaku, M. (2013). Angiogenesis and hypoxia in the kidney. Nature Reviews Nephrology 9, 211-222.
Woolf, A.S., Gnudi, L. and Long, D.A. (2009). Roles of angiopoietins in kidney development and disease. Journal of the American Society of Nephrology 20, 239-244.

Yamamoto, Y., Maeshima, Y., Kitayama, H., Kitamura, S., Takazawa, Y., Sugiyama, H., Yamasaki, Y. and Makino, H. (2004). Tumstatin peptide, an inhibitor of angiogenesis, prevents glomerular hypertrophy in the early stage of diabetic nephropathy. Diabetes 53, 1831-1840.

Zhang, S.X., Wang, J.J., Lu, K., Mott, R., Longeras, R. and Ma, J. (2006). Therapeutic potential of angiostatin in diabetic nephropathy. Journal of the American Society of Nephrology 17, 475-486.
 

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